抄録
It is already reported that glucocorticoids increase the plasma level of cholesterol by promoting the synthesis of cholesterol in the liver and by decreasing its excresion to faces. To clarify the relationships of glucocorticoids with the formation of atherosclerosis, lipoprotein patterns of steroidinduced hypercholesterolemia were analyzed, and their possible role were discussed relating to its atherogenicity. Clinically, the changes of lipoproteins in collagen disease patients who were administered glucocoriticoids were studied. Increases in serum total cholesterol, triglyceride and phospholipid level of steroid-administered patients were obseved comparing to the control people. Increased cholesterol, triglyceride and phospholipid were observed mainly in very low density lipoproteins and in high density lipoproteins, but not in low density lipoproteins.
Next, the effect of glucocorticoids administration (20mg of hydrocortisone for 14 days) on lipoprotein pattern of rabbits were examined. Serum triglyceride and phospholipid levels were significantly increased. These increases were chiefly observed in VLDL but not in LDL or HDL. Acid cholesterol esterase and acid lipase activities of steroid-administered aorta were increased, but acylcoA cholesterol acyl-transferase activity (ACAT) was not changed. These results suggested that hyperlipidemia observed in steroid-administration might not be so atherogenic from the lipoprotein profiles. The production of intermediate lipoproteins and its role were still unclear. An increase in lysosomal cholesterol esterase and unchanged ACAT activity might be against cholesterol ester accumulation in the arterial wall. Relative decrease in LDL comparing to an increase in VLDL by steroid-administration to patients, suggests that degradation system of VLDL might be impaired by glucocorticoid.
